When functioning properly, a heart maintains its own intrinsic rhythm, and is capable of pumping adequate blood throughout a circulatory system. This intrinsic rhythm is a function of intrinsic signals generated by the sinoatrial node, or SA node, located in the upper right atrium. The SA node periodically depolarizes, which in turn causes the atrial heart tissue to depolarize such that right and left atria contract as the depolarization travels through the atrial heart tissue. The atrial depolarization signal is also received by the atrioventricular node, or AV node, which, in turn, triggers a subsequent ventricular depolarization signal that travels through and depolarizes the ventricular heart tissue causing the right and left ventricles to contract.
Some patients, however, have irregular cardiac rhythms, referred to as cardiac arrhythmias. Cardiac arrhythmias result in diminished blood circulation because of diminished cardiac output. Atrial fibrillation is a common cardiac arrhythmia that reduces the pumping efficiency of the heart. Atrial fibrillation is characterized by rapid, irregular, uncoordinated depolarizations of the atria. In addition to atrial fibrillation, premature contractions of the atria and ventricles can also diminish cardiac output. Frequent premature contractions may be classified as bigeminy, and this condition can lead to symptoms such as palpitations and shortness of breath. For episodes lasting several hours or days, frequent premature contractions may exacerbate other circulatory conditions of the patient. For example, premature contractions of the atria or ventricles can put a patient at increased risk of heart failure. Additionally, frequent premature ventricular contractions may lead to left ventricular dilation and increase the risk of stroke.